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Collagen-Induced Arthritis Prevent Systemic Bone Loss in Adipose

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Collagen-Induced Arthritis Prevent Systemic Bone Loss in Adipose Adipose-Derived Mesenchymal Stem Cells Prevent Systemic Bone Loss in Collagen-Induced Arthritis This information is current as Manasa G. Garimella, Supinder Kour, Vikrant Piprode, of September 27, 2021. Monika Mittal, Anil Kumar, Lekha Rani, Satish T. Pote, Gyan C. Mishra, Naibedya Chattopadhyay and Mohan R. Wani J Immunol 2015; 195:5136-5148; Prepublished online 4 November 2015; Downloaded from doi: 10.4049/jimmunol.1500332 http://www.jimmunol.org/content/195/11/5136 Supplementary http://www.jimmunol.org/content/suppl/2015/11/04/jimmunol.150033 http://www.jimmunol.org/ Material 2.DCSupplemental References This article cites 47 articles, 10 of which you can access for free at: http://www.jimmunol.org/content/195/11/5136.full#ref-list-1 Why The JI? Submit online. by guest on September 27, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Author Choice Freely available online through The Journal of Immunology Author Choice option Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Adipose-Derived Mesenchymal Stem Cells Prevent Systemic Bone Loss in Collagen-Induced Arthritis Manasa G. Garimella,* Supinder Kour,* Vikrant Piprode,* Monika Mittal,† Anil Kumar,* Lekha Rani,* Satish T. Pote,* Gyan C. Mishra,* Naibedya Chattopadhyay,† and Mohan R. Wani* Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammatory synovitis leading to joint destruction and systemic bone loss. The inflammation-induced bone loss is mediated by increased osteoclast formation and function. Current antirheumatic therapies primarily target suppression of inflammatory cascade with limited or no success in controlling progres- sion of bone destruction. Mesenchymal stem cells (MSCs) by virtue of their tissue repair and immunomodulatory properties have shown promising results in various autoimmune and degenerative diseases. However, the role of MSCs in prevention of bone destruction in RA is not yet understood. In this study, we investigated the effect of adipose-derived MSCs (ASCs) on in vitro Downloaded from formation of bone-resorbing osteoclasts and pathological bone loss in the mouse collagen-induced arthritis (CIA) model of RA. We observed that ASCs significantly inhibited receptor activator of NF-kB ligand (RANKL)–induced osteoclastogenesis in both a contact-dependent and -independent manner. Additionally, ASCs inhibited RANKL-induced osteoclastogenesis in the presence of proinflammatory cytokines such as TNF-a, IL-17, and IL-1b. Furthermore, treatment with ASCs at the onset of CIA significantly reduced clinical symptoms and joint pathology. Interestingly, ASCs protected periarticular and systemic bone loss in CIA mice by maintaining trabecular bone structure. We further observed that treatment with ASCs reduced osteoclast precursors in bone http://www.jimmunol.org/ marrow, resulting in decreased osteoclastogenesis. Moreover, ASCs suppressed autoimmune T cell responses and increased the percentages of peripheral regulatory T and B cells. Thus, we provide strong evidence that ASCs ameliorate inflammation-induced systemic bone loss in CIA mice by reducing osteoclast precursors and promoting immune tolerance. The Journal of Immunology, 2015, 195: 5136–5148. uman rheumatoid arthritis (RA) is an autoimmune disease myeloid precursors of monocyte/macrophage lineage in the pres- characterized by chronic inflammatory synovitis and pro- ence of receptor activator of NF-kBligand(RANKL)andM-CSF H duction of autoantibodies and several proinflammatory (2). The proinflammatory milieu of the arthritic synovium leads to by guest on September 27, 2021 cytokines, which together lead to joint destruction (1). Inflammation- aberrant differentiation and activation of osteoclasts, resulting in induced bone destruction is a key pathological feature of RA, massive bone loss (3). Chronic inflammation also shifts the equi- mediated by osteoclasts. Osteoclasts are formed by the fusion of librium of bone remodeling toward increased bone resorption rather than formation, leading subsequently to systemic osteopenia asso- ciated with an enhanced risk for osteoporotic fractures (4). Current *National Centre for Cell Science, Ganeshkhind, Pune 411 007, India; and †Division of Endocrinology, Council of Scientific and Industrial Research–Central antirheumatic therapies primarily target the suppression of inflam- Drug Research Institute, Lucknow 226 031, India matory cascade with varying success in limiting the progression of Received for publication February 10, 2015. Accepted for publication September 30, bone destruction (5). Therefore, better therapeutic agents are needed 2015. affecting both inflammatory processes and skeletal damage. This work was supported by Department of Biotechnology, India Grant BT/HRD/34/ Mesenchymal stem cells (MSCs) are adult multipotent non- 01/2009 (to M.R.W.), as well as Council of Scientific and Industrial Research, New hematopoietic stem cells of mesodermal origin that can differen- Delhi, India Grant BSC0201 (to N.C.). M.G.G. is the recipient of a senior research fellowship from the Council for Scientific and Industrial Research, New Delhi, India. tiate into cells of both mesenchymal and nonmesenchymal lineages Address correspondence and reprint requests to Dr. Mohan R. Wani, National Centre (6, 7). Initially identified from bone marrow, MSCs have been iso- for Cell Science, Savitribai Phule Pune University Campus, Ganeshkhind Road, Pune lated from various sources, including adipose tissue, gingiva, um- 411 007, India. E-mail address: [email protected] bilical cord, and many other adult tissues (8). In addition to their The online version of this article contains supplemental material. regenerative potential, they exert profound immunomodulation by Abbreviations used in this article: ASC, adipose-derived mesenchymal stem cell; affecting proliferation, differentiation, and maturation of various im- BMD, bone mineral density; Breg, regulatory B cell; BV/TV, trabecular bone volume fraction; CFU-F, CFU-fibroblast; CIA, collagen-induced arthritis; CII, collagen type mune cell types (9). MSCs are also known to home to the site of II; CM, conditioned medium; Conn. D, connectivity density; Cs. Th, cross-sectional injury or inflammation and contribute to tissue repair processes lo- thickness; mCT, microcomputed tomography; Ct. BMD, cortical BMD; CTR, calci- tonin receptor; DC-STAMP, dendritic cell–specific transmembrane protein; dLN, cally through trophic factors (10). Because of the unique combination draining lymph node; MMP, matrix metalloproteinase; MNC, multinuclear cell; of these properties, MSCs are being widely studied in clinical trials of MSC, mesenchymal stem cell; OCP, osteoclast precursor; RA, rheumatoid arthritis; various autoimmune disorders and degenerative diseases (11, 12). RANK, receptor activator of NF-kB; RANKL, receptor activator of NF-kB ligand; rm, recombinant murine; Tb. BMD, trabecular BMD; Tb. N, trabecular number; Despite several conflicting reports, MSCs from various tissues Tb. Sp, trabecular separation; Tb. Th, trabecular thickness; TRAP, tartrate-resistant have shown protective effect in reducing autoimmune and inflam- acid phosphatase; Treg, regulatory T cell. matory processes in preclinical models of RA (13–15). However, This article is distributed under The American Association of Immunologists, Inc., the role of MSCs in protecting skeletal component of arthritis, in- Reuse Terms and Conditions for Author Choice articles. cluding pathological bone loss and the bone-resorbing osteoclasts, Copyright Ó 2015 by The American Association of Immunologists, Inc. 0022-1767/15/$25.00 has not been well studied. Also, earlier studies on the role of MSCs www.jimmunol.org/cgi/doi/10.4049/jimmunol.1500332 The Journal of Immunology 5137 in osteoclast differentiation are conflicting, with both stimulatory cultured in a 60-mm petri dish for 7–10 d followed by formalin fixation (16, 17) as well as inhibitory (18, 19) effects. Therefore, in the and staining with hematoxylin. Cultures were observed for colonies with present study, we investigated the effect of MSCs on the differen- aggregates of 50 or more cells using a bright-field microscope and were scored as CFU-F. tiation of bone-resorbing osteoclasts and inflammation-induced bone loss in the mouse collagen-induced arthritis (CIA) model. In vitro osteogenic, adipogenic, and chondrogenic We used syngeneic adipose-derived MSCs (ASCs) for our study differentiation of ASCs because of their ease of isolation and relative abundance. Induction of osteoblast, adipocyte, and chondrocyte differentiation was In this study, we found that ASCs inhibited RANKL-induced performed as described previously (21). For osteoblast differentiation, 3 2 osteoclast differentiation in vitro in both a contact-dependent and monolayer cultures of mouse ASCs (2–5 3
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